Myocarditis.

FFU
Medical Faculty
July lectures 2020
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 Myocarditis.
• Acute or chronic inflammation of the myocardium is characterized by
inflammatory cell infiltrates, myocyte necrosis, or myocyte degeneration
and may be caused by infectious, connective tissue, granulomatous, toxic,
or idiopathic processes.
• There may be associated systemic manifestations of the disease and on
occasion the endocardium or pericardium is involved.

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• Patients may be asymptomatic,have nonspecific prodromal symptoms, or
present with overt congestive heart failure, compromising arrhythmias, or
sudden death.
• It is thought that viral infections are the most common etiology though
myocardial toxins, drug exposures, hypersensitivity reactions, and
immune disorders may also lead to myocarditis .

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 ETIOLOGY AND EPIDEMIOLOGY.
• Viral Infections:
• Coxsackievirus and other enteroviruses, adenovirus, parvovirus, Epstein-
Barr virus, and cytomegalovirus are the most common causative agents in
children, though most known viral agents have been reported.
• In Asia, hepatitis C virus appears to be significant as well.
• The true incidence of viral myocarditis is unknown as mild cases likely
very often go undetected.

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• The disease is typically sporadic but may be epidemic. Manifestations are,
to some degree, age dependent: in infants, viral myocarditis can be
fulminant; in children, it often will occur as an acute, myopericarditis with
congestive heart failure; and in older children and adolescents,
• it may present with signs and symptoms of acute or chronic congestive
heart failure.

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 Bacterial Infections.
• Bacterial myocarditis has become far less common with the advent of
advanced public health measures, which have minimized infectious causes
such as diphtheria.
• Diphtheritic myocarditis is unique as bacterial toxin may produce
circulatory collapse and toxic myocarditis characterized by
atrioventricular block, bundle branch block, or ventricular ectopy.

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• Any overwhelming systemic bacterial infection can manifest with
circulatory collapse and shock with evidence of myocardial dysfunction
characterized by tachycardia, gallop rhythm, and low cardiac output.
• Additional nonviral infectious causes of myocarditis include rickettsia,
protozoa, parasitic infections, and fungal disease.

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 PATHOPHYSIOLOGY.
Myocarditis is characterized by myocardial inflammation, injury or necrosis,
and ultimately fibrosis.
Cardiac enlargement and diminished systolic function occur as a direct result of
the myocardial damage.
Typical signs of congestive heart failure occur and may progress rapidly to
shock, atrial or ventricular arrhythmias, and sudden death.
• The final result of viral-associated inflammation can be dilated
cardiomyopathy.
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 CLINICAL MANIFESTATIONS.
• Manifestations of myocarditis range from asymptomatic or nonspecific
generalized illness to acute cardiogenic shock and sudden death.
• Infants and young children more often have a fulminant presentation with
fever, respiratory distress, tachycardia, hypotension, gallop rhythm, and
cardiac murmur.
• Associated findings may include a rash or evidence of end organ
involvement such as hepatitis or aseptic meningitis.

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• Patients with acute or chronic myocarditis may present with chest discomfort,
fever, palpitations, easy fatigability, or syncope/near syncope.
• Cardiac findings include overactive precordial impulse, gallop rhythm, and an
apical systolic murmur of mitral insufficiency.
• In patients with associated pericardial disease, a rub may be noted.
• Hepatic enlargement, peripheral edema, and pulmonary findings such as
wheezes or rales may be present in patients with decompensated congestive
heart failure.
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 DIAGNOSIS.
• ECG changes are nonspecific and may include sinus tachycardia, atrial or
ventricular arrhythmias, heart block, diminished QRS voltages, and
nonspecific ST and T-wave changes, often suggestive of acute ischemia.
• Chest X-ray in severe, symptomatic cases reveal cardiomegaly, pulmonary
vascular prominence, overt pulmonary edema, or pleural effusions.
• Echo. often shows diminished ventricular systolic function, cardiac
chamber enlargement, mitral insufficiency, and occasionally, evidence of
pericardial infusion.
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• Endomyocardial biopsy may be useful in identifying inflammatory cell
infiltrates or myocyte damage and performing molecular viral analysis
using (PCR) techniques.
• Catheterization and biopsy, although not without risk (perforation and
arrhythmias), should be performed by experienced personnel in patients
suspected to have myocarditis or if there is strong suspicion for unusual
forms of cardiomyopathy such as storage diseases or mitochondrial
defects.
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 Treatment.
Primary therapy for acute myocarditis is supportive .
Acutely, the use of inotropic agents, preferably milrinone, should be entertained
but used with caution because of their proarrhythmic potential.
Diuretics are often required as well.
If in extremis, mechanical ventilatory support and mechanical circulatory
support with ventricular assist device implantation or ECMO may be needed to
stabilize the patient’s hemodynamic status and act as a bridge to recovery or
cardiac transplantation.
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• Diuretics, angiotensin-converting enzyme inhibitors, and angiotensin
receptor blockers are of use in patients with compensated congestive heart
failure in the outpatient setting, but may be contraindicated in those
presenting with fulminant heart failure and cardiovascular collapse.
• In patients manifesting with significant atrial or ventricular arrhythmias,
specific antiarrhythmic agents (for example, amiodarone) should be
administered and ICD placement considered.

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• Intravenous immune globulin may have a role in the treatment of acute or
fulminant myocarditis and corticosteroids have been reported to improve
cardiac function, but the data are not convincing in children.
• Relapse has been noted in patients receiving immunosuppression who
have been weaned from support.
• There are no studies to recommend specific antiviral therapies for
myocarditis

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 Thanks for your attention..

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